Table_1_Association between blood ethylene oxide levels and periodontitis risk: a population-based study.DOCX

BackgroundThe etiopathogenesis of periodontitis is closely associated with environmental conditions. However, the relationship between ethylene oxide exposure and periodontitis risk remains unclear.MethodsWe selected qualified participants from National Health and Nutrition Examination Survey (NHANES) 2013–2014. Periodontitis was identified according to the criteria of the Community Periodontal Index (CPI), Centers for Disease Control and Prevention (CDC)/American Academy of Periodontology (AAP) definition. Ethylene oxide exposure was quantified by hemoglobin adducts of ethylene oxide (HbEO) levels. Log2-transformation was used to normalize HbEO levels. We designed three logistic regression models to explore potential relationship between HbEO and periodontitis. Restricted cubic spline (RCS) and subgroup analysis were also conducted with all covariates adjusted. We performed multivariable linear regression to appraise the association between the risk of periodontitis and different indicators of inflammation, including white blood cells, neutrophils, lymphocytes, and monocytes. Mediation analysis was subsequently performed to examine whether ethylene oxide exposure contributed to periodontitis development through systemic body inflammation.ResultsA total of 1,065 participants aged more than 30 were incorporated in this study. We identified that participants with higher HbEO levels showed increased risk of periodontitis after adjusting for all covariates (OR = 1.49, 95% CI: 1.14, 1.95, p = 0.0014). The results of subgroup analysis remained stable. The restricted cubic spline (RCS) curve also revealed a non-linear correlation between log2-transformed HbEO levels with the risk of periodontitis (p for nonlinear ConclusionParticipants with higher ethylene oxide exposure showed higher risk of periodontitis, which was partially mediated by systemic body inflammation. More well-designed longitudinal studies should be carried out to validate this relationship.</p

Synthesis of NaHS zeolite using microwave assisted alkali activation of coal fly ash: preparation, mechanism, application

High value-added NaHS zeolite was prepared using the microwave-assisted alkali fusion hydrothermal method from industrial solid waste coal fly ash as raw material without adding silicon and aluminum sources. The effect of mass ratio of alkali to coal fly ash, crystallization temperature, and crystallization time on the preparation of NaHS zeolite was investigated. The NaHS zeolite was characterized using XRD, SEM, BET, and FT-IR. The experimental results showed that the NaHS zeolite with complete crystal structure could be synthesized at m(sodium hydroxide):m(coal fly ash) = 2:1, crystallization temperature of 140°C, and crystallization time of 48 h. The prepared HS zeolite had high purity, complete crystal structure, and uniform grain size (2 μm). The NaHS zeolite was beneficial for CO2 adsorption properties with 110.9 cm3/g at 25°C.</p

The B-term genes make up potential common molecular pathways between gastric cancer and anandamide.

<p>The B-term genes make up potential common molecular pathways between gastric cancer and anandamide.</p

The effect of anandamide on cell cycle regulators.

<p>A. Analysis of differential gene expression profiling in the AGS cells with the presence and absence of anandamide. Data were obtained from three samples each group. The differential gene with average Changes(fold >2) after exposure to anandamide (10 µM) for 24 h were picked up, the graphs show the fold changes of these cell cycle related genes. B. Effect of anandamide on the expression of the cell cycle regulators. Cells were harvested after anandamide (10 µM) or ethanol solvent treatment for 24h and analyzed by western blotting with antibodies against Chk1, p-Chk1, CDC25A, and CyclinB1. C. The results of western blotting were normalized against β-actin. Fold changes of these proteins were determined by comparison with levels measured in control ethanol treated cells. Data are presented as mean ± SD (n  =  3), * indicates <i>p<0.05</i> compared with control.</p

The predicted relationship between gastric cancer and anandamide.

<p>The predicted relationship between gastric cancer and anandamide.</p

<i>In Situ</i> Reaction-Generated Aldehyde-Scavenging Polypeptides-Curcumin Conjugate Nanoassemblies for Combined Treatment of Spinal Cord Injury

The microenvironment after traumatic spinal cord injury (SCI) involves complex pathological processes, including elevated oxidative stress, accumulated reactive aldehydes from lipid peroxidation, excessive immune cell infiltration, etc. Unfortunately, most of current neuroprotection therapies cannot cope with the intricate pathophysiology of SCI, leading to scant treatment efficacies. Here, we developed a facile in situ reaction-induced self-assembly method to prepare aldehyde-scavenging polypeptides (PAH)-curcumin conjugate nanoassemblies (named as PFCN) for combined neuroprotection in SCI. The prepared PFCN could release PAH and curcumin in response to oxidative and acidic SCI microenvironment. Subsequently, PFCN exhibited an effectively neuroprotective effect through scavenging toxic aldehydes as well as reactive nitrogen and oxygen species in neurons, modulating microglial M1/M2 polarization, and down-regulating the expression of inflammation-related cytokines to inhibit neuroinflammation. The intravenous administration of PFCN could significantly ameliorate the malignant microenvironment of injured spinal cord, protect the neurons, and promote the motor function recovery in the contusive SCI rat model

The effect of anandamide on gastric cancer cells.A.The structures of tetrahydrocannabinol and anandamide.

<p>Anandamide functional groups include amides, esters, and ethers of long-chain polyunsaturated fatty acids, and structurally share critical pharmacophores with D-9-tetrahydrocannabinol (THC). B.Anandamide treatment inhibits the proliferation of gastric cancer cells. BGC823, SGC7901, AGS, and N87 cells were treated with synthetic anandamide at concentrations of 0, 50, and 100 µM for 24 h. The proliferation rate was detected by the MTT assay. Cells treated with vehicle of ethanol were employed as a control. Data are presented as mean ± SD (n = 3), * indicates <i>p<0.01</i> compared with control. C.Anandamide treatment inhibited the proliferation of AGS and N87 cells. AGS and N87 cells were treated with synthetic anandamide with increasing concentrations of 0, 0.01, 0.1, 1, and 10 µM for 24 h. The proliferation rate was detected by MTT assay. Data are presented as mean ± SD (n = 3). * indicates <i>p<0.01</i> compared with control. D.The effect of anandamide on apoptosis in AGS and N87 cells. AGS and N87 cells were treated with anandamide at a concentration of 10 µM for 24 h. Apoptosis were analyzed by flow cytometry. Cells treated with vehicle were used as a control.</p

The top-level MeSH categories of the stop-terms list.

<p>The top-level MeSH categories of the stop-terms list.</p

The filtered B-terms made up a molecular regulatory network.

<p>The critical genes of the B-terms were collected and using Mas 3.0 annotation system (Capital Bio <a href="http://bioinfo.capitalbio.com/mas3/" target="_blank">http://bioinfo.capitalbio.com/mas3/</a>) a molecular network was constructed. The abbreviations represented different genes involved in some important signal pathways related to both gastric cancer and anandamide. e.g., The PTGS2 gene codes for COX-2, an enzyme responsible for inflammation and pain, was reported that its mutationsmay be responsible for a higher risk of gastric cancer, in the meantime, COX-2 also metabolizes anandamide forming prostaglandin-ethanolamides (PG-EA). The numbers and color on the lines connected genes means the counts of the gene appeared in different signal pathways in three biological pathway database including Biocarta, GenMAPP andKEGG (Red: Biocarta; Green:GenMAPP; Blue: KEGG).</p

Effect of anandamide on cell cycle distribution of gastric cancer cells.

<p>A. The AGS cells at the period logarithmic growth were incubated with 10 µM anandamide or ethanol solvent for 24 h. The cell cycle phase was analyzed with flow cytometry. Cells treated with anandamide experienced a significant G2 block. B. N87 cells were treated with anandamide (10 µM) for 24 hand then halted in the G2 phase of cell cycle. The control cells were treated with ethanol solvent. The cell cycle phase was analyzed with flow cytometry. C. The AGS Cells arrested at G1 phase by serum starvation were released at t  =  0h and incubated with anandamide(10 µM) or ethanol. The cells were collected at 6h, 12h, and 24 h, and DNA contents were analyzed by flow cytometry. The percentage of cells in each phase of cell cycle displayed anandamide causing G2/M phases at 24h. Graphs are representative of 2 independent experiments with similar results. D. The N87 cells were synchronized in G1 phase by serum starvation and were released at t = 0, simultaneously they were treated with anandamide(10 µM) or ethanol. The cells were harvested at 6h, 12h, 24h and prepared for flow cytometry analysis. Graphs are representative of 2 independent experiments with similar results.</p